Abstract

Opiate abuse increases susceptibility to bacterial infection. However, if the intestine can be a potential source of bacterial infections in opiate abusers is not fully elucidated. Using an opiate abuse model, where mice were chronically treated with morphine or placebo pellet, we found that morphine treatment induced bacterial translocation and led to bacteraemia. After morphine exposure, group D Entercocci and coagulase negative Staphylococci were detected in the mesenteric lymph nodes and lungs. Morphine treatment enhanced bacterial growth in the intestine, and that such increased in bacteria was in direct proportion to coagulase-negative staphylococcal bacteraemia. Furthermore, our preliminary findings showed that morphine treatment modulated intestinal intraepithelial gammadelta T cells and impaired intestinal permeability. Moreover, morphine treatment induced dysfunction in intestinal intraepithelial gammadelta T cells was associated with the absence of phosphorylation of occludin and lack of claudin-3 and zona occludens-1 (ZO-1) proteins in tight junction complexes. Our studies suggest that bacterial translocation and bacteraemia occurs in opiate abusers, either on account of a breach of the mucosal barrier, impaired host immune defense, and/or bacterial overgrowth creating an ecologic imbalance in the indigenous intestinal microflora. Supported by R01 DA12104, P50 DA11806, and R03 DA023353.